Bio: Hui-Li Wang is a professor at School of Food and Biological Engineering at Hefei University of Technology. Her research focuses on understanding the molecular and cellular mechanisms underlying the synaptic plasticity, neuro-circuitry formation and epigenetic regulation during environmental neurotoxins induced neurobehavior dysfunctions. She has won various awards, scholarships or recognitions such as “The National Innovation Talent Support Program”, “New Century Excellent Talents in University”, and “a rising star”in the field of toxicology by the Royal Society of Chemistry. In addition to serving as Associate Editor at Current Research in Toxicology, she is also currently on the editorial board of eLife, Food Science and Human Wellness, and Food and Chemical Toxicology.

Abstract: There is robust evidence that environmental risk factors impact cognitive performance. In this talk, the effect of the environmental risk factor Pb on susceptibility to cognition and mood dysfunctions will be discussed. Here, it is demonstrated that Pb exposure increases the susceptibility to these deficits, with the impairment of hippocampal excitatory neurons as the underlying cause. Furthermore, Pb exposure increased HDAC2 levels in CA1 excitatory neurons, a crucial epigenetic factor for reprogramming synaptic plasticity and memory formation. These deficits could be rescued via Hdac2-cKO in CA1 excitatory neurons. Additionally, Hdac2-cKO reversed the reduction in miniature excitatory postsynaptic currents (mEPSC), Ca2+ signaling, and spine density caused by Pb in CA1 excitatory neurons. In terms of the mechanistic insight, Hdac2-cKO reversed the downregulated expression of TRPC6, LRP2, VGLUT1, NMDAR1, NMDAR2B, AMPAR2, and PSD95 in CA1 excitatory neurons. In conclusion, Pb causes nonspatial memory deficits and synaptic plasticity impairments by increasing HDAC2 in hippocampal CA1 excitatory neurons, providing a new reference for the prevention and treatment of memory deficits induced by environmental cues.